ArticleThe FEBS journal2023
KIAA0317 regulates SOCS1 stability to ameliorate colonic inflammation.
Article in The FEBS journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- DTX3L promotes ovarian cancer progression and cisplatin resistance by activating JAK1/STAT1/OAS3 pathway.Scientific reports · 2026Article
- SOCS1 improves abnormal IgA galactosylation in IgA nephropathy by regulating the TLR9/MyD88 pathway.Immunologic research · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Dysregulated cytokine signalling is a hallmark of inflammatory bowel diseases. Inflammatory responses of the colon are regulated by the suppressor of cytokine signalling (SOCS) proteins. SOCS1 is a key member of this family, and its function is critical in maintaining an appropriate inflammatory response through the JAK/STAT signalling pathway. Dysregulation of SOCS1 protein has been identified as a causal element in colonic inflammatory diseases. Despite this, it remains unclear how SOCS1 protein is regulated. Here, we identify that SOCS1 protein is targeted for degradation by the ubiquitin proteasome system, mediated by the E3 ubiquitin ligase KIAA0317 during experimental colonic inflammation. We characterize the mechanism of protein-protein interaction and ubiquitin conjugation to SOCS1 and demonstrate that the modulation of SOCS1 protein level leads to stark effects on JAK/STAT inflammatory signalling. Together, these results provide insight into the regulation of colonic inflammation through a new mechanism of ubiquitin-based control of SOCS1 protein.
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Registered trials
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